The caveolae‐associated coiled‐coil protein, NECC2, regulates insulin signalling in Adipocytes

Adipocyte dysfunction in obesity is commonly associated with impaired insulin signalling in adipocytes and insulin resistance. Insulin signalling has been associated with caveolae, which are coated by large complexes of caveolin and cavin proteins, along with proteins with membrane‐binding and remodelling properties. Here, we analysed the regulation and function of a component of caveolae involved in growth factor signalling in neuroendocrine cells, neuroendocrine long coiled‐coil protein‐2 (NECC2), in adipocytes. Studies in 3T3‐L1 cells showed that NECC2 expression increased during adipogenesis. Furthermore, NECC2 co‐immunoprecipitated with caveolin‐1 (CAV1) and exhibited a distribution pattern similar to that of the components of adipocyte caveolae, CAV1, Cavin1, the insulin receptor and cortical actin. Interestingly, NECC2 overexpression enhanced insulin‐activated Akt phosphorylation, whereas NECC2 downregulation impaired insulin‐induced phosphorylation of Akt and ERK2. Finally, an up‐regulation of NECC2 in subcutaneous and omental adipose tissue was found in association with human obesity and insulin resistance. This effect was also observed in 3T3‐L1 adipocytes exposed to hyperglycaemia/hyperinsulinemia. Overall, the present study identifies NECC2 as a component of adipocyte caveolae that is regulated in response to obesity and associated metabolic complications, and supports the contribution of this protein as a molecular scaffold modulating insulin signal transduction at these membrane microdomains.La disfunción de los adipocitos en la obesidad se asocia comúnmente con la alteración de la señalización de la insulina en los adipocitos y la resistencia a la insulina. La señalización de la insulina se ha asociado con las caveolas, que están recubiertas por grandes complejos de proteínas de caveolina y cavina, junto con proteínas con propiedades de remodelación y unión a la membrana. Aquí, analizamos la regulación y la función de un componente de las caveolas involucrado en la señalización del factor de crecimiento en las células neuroendocrinas, la proteína 2 neuroendocrina de espiral larga (NECC 2 ) , en los adipocitos. Los estudios en células 3T3‐L1 mostraron que la expresión de NECC 2 aumentó durante la adipogénesis. Además, NECC 2 co‐inmunoprecipitado con caveolina‐1 ( CAV1) y mostró un patrón de distribución similar al de los componentes de las caveolas adipocitarias, CAV 1, Cavin1, el receptor de insulina y la actina cortical. Curiosamente, la sobreexpresión de NECC 2 mejoró la fosforilación de Akt activada por insulina, mientras que la regulación negativa de NECC 2 perjudicó la fosforilación de Akt y ERK 2 inducida por insulina . resistencia a la insulina. Este efecto también se observó en adipocitos 3T3‐L1 expuestos a hiperglucemia/hiperinsulinemia. En general, el presente estudio identifica NECC2 como un componente de las caveolas de los adipocitos que se regula en respuesta a la obesidad y las complicaciones metabólicas asociadas, y respalda la contribución de esta proteína como un andamio molecular que modula la transducción de señales de insulina en estos microdominios de membrana

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The caveolae-associated coiled-coil protein, NECC2, regulates insulin signalling in Adipocytes

Adipocyte dysfunction in obesity is commonly associated with impaired insulin sig-nalling in adipocytes and insulin resistance. Insulin signalling has been associatedwith caveolae, which are coated by large complexes of caveolin and cavin proteins,along with proteins with membrane‐binding and remodelling properties. Here, weanalysed the regulation and function of a component of caveolae involved in growthfactor signalling in neuroendocrine cells, neuroendocrine long coiled‐coil protein‐2(NECC2), in adipocytes. Studies in 3T3‐L1 cells showed that NECC2 expressionincreased during adipogenesis. Furthermore, NECC2 co‐immunoprecipitated withcaveolin‐1 (CAV1) and exhibited a distribution pattern similar to that of the compo-nents of adipocyte caveolae, CAV1, Cavin1, the insulin receptor and cortical actin.Interestingly, NECC2 overexpression enhanced insulin‐activated Akt phosphoryla-tion, whereas NECC2 downregulation impaired insulin‐induced phosphorylation ofAkt and ERK2. Finally, an up‐regulation ofNECC2in subcutaneous and omental adi-pose tissue was found in association with human obesity and insulin resistance. Thiseffect was also observed in 3T3‐L1 adipocytes exposed to hyperglycaemia/hyperin-sulinemia. Overall, the present study identifies NECC2 as a component of adipocytecaveolae that is regulated in response to obesity and associated metabolic complica-tions, and supports the contribution of this protein as a molecular scaffold modulat-ing insulin signal transduction at these membrane microdomains

The caveolae-associated coiled-coil protein, NECC2, regulates insulin signalling in Adipocytes

Adipocyte dysfunction in obesity is commonly associated with impaired insulin sig-nalling in adipocytes and insulin resistance. Insulin signalling has been associatedwith caveolae, which are coated by large complexes of caveolin and cavin proteins,along with proteins with membrane‐binding and remodelling properties. Here, weanalysed the regulation and function of a component of caveolae involved in growthfactor signalling in neuroendocrine cells, neuroendocrine long coiled‐coil protein‐2(NECC2), in adipocytes. Studies in 3T3‐L1 cells showed that NECC2 expressionincreased during adipogenesis. Furthermore, NECC2 co‐immunoprecipitated withcaveolin‐1 (CAV1) and exhibited a distribution pattern similar to that of the compo-nents of adipocyte caveolae, CAV1, Cavin1, the insulin receptor and cortical actin.Interestingly, NECC2 overexpression enhanced insulin‐activated Akt phosphoryla-tion, whereas NECC2 downregulation impaired insulin‐induced phosphorylation ofAkt and ERK2. Finally, an up‐regulation ofNECC2in subcutaneous and omental adi-pose tissue was found in association with human obesity and insulin resistance. Thiseffect was also observed in 3T3‐L1 adipocytes exposed to hyperglycaemia/hyperin-sulinemia. Overall, the present study identifies NECC2 as a component of adipocytecaveolae that is regulated in response to obesity and associated metabolic complica-tions, and supports the contribution of this protein as a molecular scaffold modulat-ing insulin signal transduction at these membrane microdomains